Excessive salt-ingestion in man has long been associated with an increased risk of developing hypertension, yet the mechanisms by which salt acts are poorly understood. In the Dahl rat model, Salt-Sensitive rats (DS) develop elevated blood pressures on a high salt (HS) diet while Salt-Resistant rats (DR) remain normotensive. Recent research has suggested that there is a significant neurogenic contribution to the development of hypertension in DS rats. The arterial and cardiopulmonary baroreflexes of DS rats are depressed even before exposure to high salt and the subsequent development of hypertension. This project will test whether abnormal function of the cardiovascular mechanoreceptors contributes to these decreases in baroreflex sensitivity in DS rats. I will use two in vitro preparations to study quantitatively the response characteristics of aortic arch baroreceptors and cardiopulmonary mechanoreceptors located in the superior vena cava just outside the right atrium. This in vitro approach allows a much more precise control of experimental conditions including reproducible, well-defined pressure inputs and ionic environment. In addition, the geometry of the vessel walls in which these mechanoreceptors are found can be closely approximated by a simple right cylinder so that the contribution of vessel wall distensibility and mechanics can be assessed through measurements of vessel diameter. Single mechanoreceptors will be tested for steady-state discharge characteristics including threshold and suprathreshold sensitivity, for rapid resetting to changes in the conditioning pressure and for sensitivity to changes in external ionic concentrations. Of particular importance are the comparisons of an inbred, nonselected strain of control rats (Sprague-Dawley) to both DS and DR and the effect of low salt and high salt diets.